| Proteomics and postgenomic technologies have found growing recent applications in reproductive biology and fertility research.Spermatogenesis and maturation are important to male reproduction.The mice deficient in the wild-type p53-induced phosphatase 1(WIP1)exhibit defects in reproductive organs.In the present study,we aimed to understand the mechanism how Wipl deficiency affects spermatogenesis and sperm maturation.The WIP1 was highly expressed in the reproductive tissues testis and epididymis.We employed the Wipl-/-mouse as study model,and we used gel-free iTRAQ LC-MS/MS quantitative proteomic analysis of the whole epididymis,including somatic tissue and sperm.A total of 8763 proteins were identified,of which 91 were significantly differentially expressed proteins in Wip1-/-mice compared to the wild type mice.Notably,the differently expression of four reproduction-related differentially expressed proteins(PRM2,ODF1,PIWIL1 and KLHL10)between the wild mice and Wipl knockout mice were confirmed by western blotting.Pathway analysis suggested that the Smac/Diablo-mediated apoptotic pathway and the SERPINA3-mediated inflammatory process may contribute to the atrophy and marked reduction of sperm in the epididymis.Network analysis of reproduction-related differentially expressed proteins revealed possible interactions of WIP1 that may affect sperm maturation,such as reduced ODF1 and PRM2 expression,and increased PIWILI expression via p53.Histological analysis showed a spermatid deficiency in the epididymis and was further confirmed in testis in Wipl-/-mice.Immunohistochemistry showed that testicular expressions of PRM2 and PIWIL1 were down-and up-regulated,respectively.In summary,WIP1 deficiency appears to cause impaired spermatogenesis in the testis and damaged sperm maturation in the epididymis.These may be attributed in part to regulation of PRM2,ODF1,PIWIL1 and associated pathways as well as the inflammatory and apoptotic pathways. |
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